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Updated: May 23, 2025

Induction of Murine Intestinal Inflammation by Adoptive Transfer of Effector CD4+CD45RBhigh T Cells into Immunodeficient Mice
Published on: April 21, 2015
STAT1 mediates the pro-inflammatory role of GBP5 in colitis
Yichen Li1,2,3, Wenxia Wang1,3,4, Ruixin Zhu5
1Department of Immunology and Microbiology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, China.
Abstract:
Previous studies establish guanylate binding protein 5 (GBP5) as a driver in the development of inflammatory bowel diseases (IBDs). Here, we aim to elucidate the mechanism underlying the pro-inflammatory role of GBP5. We observe that loss of Gbp5 causes reduced colonic inflammation and decreased numbers of innate lymphoid cells (ILCs) in colitis mice. The transcriptional alterations observed in GBP5-deficient THP-1 cells mirrored those triggered by STAT1 activation, leading to the findings that GBP5 is essential for the stimulated expression of STAT1 and its downstream effectors, including cytokines that drive the expansion of ILCs. Remarkably, over-expression of STAT1 reverses the reduced cytokine expression caused by GBP5 deficiency. While GBP5 does not directly drive gene transcription, it binds with STAT1 and facilitates its nuclear translocation, thereby enhancing the expression of STAT1 itself and its downstream effectors. Overall, GBP5 plays a pro-inflammatory role in IBD by enhancing the activity and expression of STAT1.
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